Division of Geriatric Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Chinese Medicine Department, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Gastroenterol Res Pract. 2015;2015:235017. doi: 10.1155/2015/235017. Epub 2015 Jan 22.
We explored mechanisms of vascular endothelial injury that lead to systemic multiple organ failure by detecting the soluble endothelial protein C receptor (sEPCR), von Willebrand factor (vWF), serum nitric oxide (NO), and tumor necrosis factor alpha (TNF-α) and Bcl-2 mRNA and Bax mRNA expression in a severe acute pancreatitis (SAP) rat model. Compared to controls, the levels of TNF-α, vWF, and sEPCR were significantly increased in the experimental group at 12 hours and 24 hours and the NO level was significantly decreased. After 12 hours, the aortic endothelial apoptosis index and Bax mRNA expression in aortic endothelial cells had increased in the experimental group, but Bcl-2 mRNA levels had decreased. All these changes appeared at both 12 h and 24 hours. The results indicated that vascular endothelial injury and apoptosis markers were elevated in SAP. Endothelial injury and increased apoptosis in the experimental group were related to the increased expression of TNF-α.
我们通过检测严重急性胰腺炎（SAP）大鼠模型中可溶性内皮蛋白 C 受体（sEPCR）、血管性血友病因子（vWF）、血清一氧化氮（NO）和肿瘤坏死因子-α（TNF-α）以及 Bcl-2mRNA 和 BaxmRNA 的表达，探索导致全身多器官衰竭的血管内皮损伤机制。与对照组相比，实验组在 12 小时和 24 小时时 TNF-α、vWF 和 sEPCR 水平显著升高，NO 水平显著降低。12 小时后，实验组主动脉内皮细胞的细胞凋亡指数和 BaxmRNA 表达增加，但 Bcl-2mRNA 水平降低。所有这些变化在 12 小时和 24 小时均出现。结果表明，SAP 中血管内皮损伤和细胞凋亡标志物升高。实验组的内皮损伤和增加的细胞凋亡与 TNF-α表达增加有关。
